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Hernan E. Lara - One of the best experts on this subject based on the ideXlab platform.

  • Huperzine‐A administration recovers rat Ovary Function after sympathetic stress
    Journal of neuroendocrinology, 2020
    Co-Authors: Raul Riquelme, Freddy Ruz, Artur Mayerhofer, Hernan E. Lara
    Abstract:

    Chronic cold stress affects ovarian morphology and impairs fertility in rats. It causes an ovarian polycystic Ovary (PCOS)-like phenotype, which resembles PCOS in women. The mechanism of cold stress action involves increased ovarian noradrenaline (NA) levels, which remain elevated after cessation of cold stress. By contrast, ovarian acetylcholine (ACh) levels are only transiently elevated and returned to control levels after a 28-day post stress period. Because ACh can exert trophic actions in the Ovary, we hypothesised that a sustained elevation of ovarian ACh levels by intraovarian exposure to the ACh-esterase blocker huperzine-A (Hup-A) may interfere with cold stress-induced ovarian changes. This possibility was examined in female Sprague-Dawley rats exposed to cold stress (4°C for 3 h day-1 for 28 days), followed by a 28-day period without stress. To elevate ACh, in a second group Hup-A was delivered into the Ovary of cold stress-exposed rats. A third group was not exposed to cold stress. As expected, cold stress elevated ovarian NA, reduced the number of corpora lutea and increased the number of follicular cysts. It increased plasma testosterone and oestradiol but decreased plasma levels of progesterone. In the Hup-A group, ovarian levels of both, NA and ACh, were elevated, there were fewer cysts and normal testosterone and oestradiol plasma levels were found. However, progesterone levels remained low. Most likely, low progesterone was associated with impaired mating behaviour and low pregnancy rate. We propose that elevated intraovarian levels of ACh are involved in the rescue of ovarian Function, opening a target to control ovarian diseases affecting follicular development.

  • huperzine a administration recovers rat Ovary Function after sympathetic stress
    Journal of Neuroendocrinology, 2020
    Co-Authors: Raul Riquelme, Freddy Ruz, Artur Mayerhofer, Hernan E. Lara
    Abstract:

    Chronic cold stress affects ovarian morphology and impairs fertility in rats. It causes an ovarian polycystic Ovary (PCOS)-like phenotype, which resembles PCOS in women. The mechanism of cold stress action involves increased ovarian noradrenaline (NA) levels, which remain elevated after cessation of cold stress. By contrast, ovarian acetylcholine (ACh) levels are only transiently elevated and returned to control levels after a 28-day post stress period. Because ACh can exert trophic actions in the Ovary, we hypothesised that a sustained elevation of ovarian ACh levels by intraovarian exposure to the ACh-esterase blocker huperzine-A (Hup-A) may interfere with cold stress-induced ovarian changes. This possibility was examined in female Sprague-Dawley rats exposed to cold stress (4°C for 3 h day-1 for 28 days), followed by a 28-day period without stress. To elevate ACh, in a second group Hup-A was delivered into the Ovary of cold stress-exposed rats. A third group was not exposed to cold stress. As expected, cold stress elevated ovarian NA, reduced the number of corpora lutea and increased the number of follicular cysts. It increased plasma testosterone and oestradiol but decreased plasma levels of progesterone. In the Hup-A group, ovarian levels of both, NA and ACh, were elevated, there were fewer cysts and normal testosterone and oestradiol plasma levels were found. However, progesterone levels remained low. Most likely, low progesterone was associated with impaired mating behaviour and low pregnancy rate. We propose that elevated intraovarian levels of ACh are involved in the rescue of ovarian Function, opening a target to control ovarian diseases affecting follicular development.

  • Role of stress and sympathetic innervation in the development of polycystic Ovary syndrome
    Endocrine, 2005
    Co-Authors: Monika Greiner, Alfonso Paredes, Verónica Araya, Hernan E. Lara
    Abstract:

    This article presents a review of the role of the sympathetic activity in ovarian pathologies affecting reproductive Function. We provide a succinct outline of the findings of our group in this area. The participation of stress as an etiological factor for ovarian pathologies throughout animal models and data in patients with polycystic Ovary syndrome give strong support for participation of sympathetic nerves in the Ovary Function both in normal and pathological status.

Daniel A. Gorelick - One of the best experts on this subject based on the ideXlab platform.

  • g protein coupled estrogen receptor is not required for sex determination or Ovary Function in zebrafish
    Endocrinology, 2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors α and β (ERα and ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function was normal in gper mutant ovaries compared with wild type. Our findings suggest that GPER is not required for sex determination, Ovary development, or fertility in zebrafish.

  • G Protein–Coupled Estrogen Receptor Is Not Required for Sex Determination or Ovary Function in Zebrafish
    Endocrinology, 2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors α and β (ERα and ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function was normal in gper mutant ovaries compared with wild type. Our findings suggest that GPER is not required for sex determination, Ovary development, or fertility in zebrafish.

  • G protein-coupled estrogen receptor is not required for sex determination or Ovary Function in zebrafish
    2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors alpha and beta (ERα, ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios and fertility. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function were normal in gper mutant ovaries compared to wild type. Our findings suggest that GPER is not required for sex determination, Ovary development or fertility in zebrafish.

Camerron M. Crowder - One of the best experts on this subject based on the ideXlab platform.

  • g protein coupled estrogen receptor is not required for sex determination or Ovary Function in zebrafish
    Endocrinology, 2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors α and β (ERα and ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function was normal in gper mutant ovaries compared with wild type. Our findings suggest that GPER is not required for sex determination, Ovary development, or fertility in zebrafish.

  • G Protein–Coupled Estrogen Receptor Is Not Required for Sex Determination or Ovary Function in Zebrafish
    Endocrinology, 2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors α and β (ERα and ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function was normal in gper mutant ovaries compared with wild type. Our findings suggest that GPER is not required for sex determination, Ovary development, or fertility in zebrafish.

  • G protein-coupled estrogen receptor is not required for sex determination or Ovary Function in zebrafish
    2018
    Co-Authors: Camerron M. Crowder, Shannon N Romano, Daniel A. Gorelick
    Abstract:

    Estrogens regulate vertebrate development and Function through binding to nuclear estrogen receptors alpha and beta (ERα, ERβ) and the G protein-coupled estrogen receptor (GPER). Studies in mutant animal models demonstrated that ERα and ERβ are required for normal Ovary development and Function. However, the degree to which GPER signaling contributes to Ovary development and Function is less well understood. Previous studies using cultured fish oocytes found that estradiol inhibits oocyte maturation in a GPER-dependent manner, but whether GPER regulates oocyte maturation in vivo is not known. To test the hypothesis that GPER regulates oocyte maturation in vivo, we assayed Ovary development and Function in gper mutant zebrafish. We found that homozygous mutant gper embryos developed into male and female adults with normal sex ratios and fertility. Adult mutant fish exhibited normal secondary sex characteristics and fertility. Additionally, mutant ovaries were histologically normal. We observed no differences in the number of immature versus mature oocytes in mutant versus wild-type ovaries from both young and aged adults. Furthermore, expression of genes associated with sex determination and Ovary Function were normal in gper mutant ovaries compared to wild type. Our findings suggest that GPER is not required for sex determination, Ovary development or fertility in zebrafish.

Raul Riquelme - One of the best experts on this subject based on the ideXlab platform.

  • Huperzine‐A administration recovers rat Ovary Function after sympathetic stress
    Journal of neuroendocrinology, 2020
    Co-Authors: Raul Riquelme, Freddy Ruz, Artur Mayerhofer, Hernan E. Lara
    Abstract:

    Chronic cold stress affects ovarian morphology and impairs fertility in rats. It causes an ovarian polycystic Ovary (PCOS)-like phenotype, which resembles PCOS in women. The mechanism of cold stress action involves increased ovarian noradrenaline (NA) levels, which remain elevated after cessation of cold stress. By contrast, ovarian acetylcholine (ACh) levels are only transiently elevated and returned to control levels after a 28-day post stress period. Because ACh can exert trophic actions in the Ovary, we hypothesised that a sustained elevation of ovarian ACh levels by intraovarian exposure to the ACh-esterase blocker huperzine-A (Hup-A) may interfere with cold stress-induced ovarian changes. This possibility was examined in female Sprague-Dawley rats exposed to cold stress (4°C for 3 h day-1 for 28 days), followed by a 28-day period without stress. To elevate ACh, in a second group Hup-A was delivered into the Ovary of cold stress-exposed rats. A third group was not exposed to cold stress. As expected, cold stress elevated ovarian NA, reduced the number of corpora lutea and increased the number of follicular cysts. It increased plasma testosterone and oestradiol but decreased plasma levels of progesterone. In the Hup-A group, ovarian levels of both, NA and ACh, were elevated, there were fewer cysts and normal testosterone and oestradiol plasma levels were found. However, progesterone levels remained low. Most likely, low progesterone was associated with impaired mating behaviour and low pregnancy rate. We propose that elevated intraovarian levels of ACh are involved in the rescue of ovarian Function, opening a target to control ovarian diseases affecting follicular development.

  • huperzine a administration recovers rat Ovary Function after sympathetic stress
    Journal of Neuroendocrinology, 2020
    Co-Authors: Raul Riquelme, Freddy Ruz, Artur Mayerhofer, Hernan E. Lara
    Abstract:

    Chronic cold stress affects ovarian morphology and impairs fertility in rats. It causes an ovarian polycystic Ovary (PCOS)-like phenotype, which resembles PCOS in women. The mechanism of cold stress action involves increased ovarian noradrenaline (NA) levels, which remain elevated after cessation of cold stress. By contrast, ovarian acetylcholine (ACh) levels are only transiently elevated and returned to control levels after a 28-day post stress period. Because ACh can exert trophic actions in the Ovary, we hypothesised that a sustained elevation of ovarian ACh levels by intraovarian exposure to the ACh-esterase blocker huperzine-A (Hup-A) may interfere with cold stress-induced ovarian changes. This possibility was examined in female Sprague-Dawley rats exposed to cold stress (4°C for 3 h day-1 for 28 days), followed by a 28-day period without stress. To elevate ACh, in a second group Hup-A was delivered into the Ovary of cold stress-exposed rats. A third group was not exposed to cold stress. As expected, cold stress elevated ovarian NA, reduced the number of corpora lutea and increased the number of follicular cysts. It increased plasma testosterone and oestradiol but decreased plasma levels of progesterone. In the Hup-A group, ovarian levels of both, NA and ACh, were elevated, there were fewer cysts and normal testosterone and oestradiol plasma levels were found. However, progesterone levels remained low. Most likely, low progesterone was associated with impaired mating behaviour and low pregnancy rate. We propose that elevated intraovarian levels of ACh are involved in the rescue of ovarian Function, opening a target to control ovarian diseases affecting follicular development.

Monika Greiner - One of the best experts on this subject based on the ideXlab platform.

  • Role of stress and sympathetic innervation in the development of polycystic Ovary syndrome
    Endocrine, 2005
    Co-Authors: Monika Greiner, Alfonso Paredes, Verónica Araya, Hernan E. Lara
    Abstract:

    This article presents a review of the role of the sympathetic activity in ovarian pathologies affecting reproductive Function. We provide a succinct outline of the findings of our group in this area. The participation of stress as an etiological factor for ovarian pathologies throughout animal models and data in patients with polycystic Ovary syndrome give strong support for participation of sympathetic nerves in the Ovary Function both in normal and pathological status.